Published online Dec 14, 2020. doi: 10.3748/wjg.v26.i46.7352
Peer-review started: September 27, 2020
First decision: October 17, 2020
Revised: October 28, 2020
Accepted: November 4, 2020
Article in press: November 4, 2020
Published online: December 14, 2020
Processing time: 77 Days and 17 Hours
Vitamin D has been proved to be associated with the pathogenesis of ulcerative colitis (UC) due to its role in regulating immunity. Increased Jumonji domain-containing 3 (Jmjd3) can aggravate colitis in mice by demethylating repressive trimethylated H3 lysine 27 (H3K27me3). However, it is unknown whether Jmjd3 and H3K27me3 are associated with the pathogenesis of UC, and the association between vitamin D receptor (VDR) and the Jmjd3 pathway remains unclear.
There is limited evidence on the influence of vitamin D on disease activity in Chinese patients with active UC. The expression of Jmjd3 and H3K27me3 in the intestinal mucosa of patients with UC has not been studied. Research on the relationship between VDR and the Jmjd3 is helpful to understand the possible pathogenesis of UC.
To investigate the expression of serum vitamin D, VDR, Jmjd3 and H3K27me3 in UC patients and controls, and to determine the correlation between VDR and the Jmjd3 pathway.
In this study, 100 patients with active UC and 56 healthy controls were enrolled. Serum C-reactive protein and alkaline phosphatase levels were determined by immunoturbidimetry. White blood cell and hemoglobin were detected using a Sysmex XN-9000 automatic hematology analyzer. The content of serum vitamin D was determined by radioimmunoassay. The expression of VDR, Jmjd3 and H3K27me3 in intestinal mucosa was detected by immunohistochemistry.
Patients with active UC had lower levels of vitamin D than controls. Serum vitamin D level was negatively correlated with disease activity in the UC cohort. VDR expression in the mucosa of UC patients was reduced compared with normal tissues and negatively correlated with disease activity. Simultaneously, Jmjd3 expression increased, while H3K27me3 decreased in UC patients. The Jmjd3 level was negatively correlated with the level of VDR and H3K27me3, while the VDR level was positively correlated with H3K27me3 in all subjects.
This report outlines an inverse correlation of vitamin D and VDR with disease activity in active UC patients in which both Jmjd3 and H3K27me3 are presumedly participated.
More quantitative measures will be performed for detecting VDR, Jmjd3 and H3K27me3 in UC patients. Clinical trials of vitamin D supplementation should be carried out, which will contribute to a better understanding of the effect of vitamin D on UC.